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Clinical Assessment and Management of Spasticity and Contractures in Traumatic Brain Injury
Published in Anand D. Pandyan, Hermie J. Hermens, Bernard A. Conway, Neurological Rehabilitation, 2018
An interesting and clinically challenging sequela of traumatic brain injury that is often observed in those in vegetative or minimally conscious states is paroxysmal sympathetic hyperactivity, a prominent feature of which is posturing either in the decorticate or decerebrate pattern. An international, multidisciplinary consensus group (Baguley et al. 2014) described this syndrome as:
Rehabilitation of the child with injuries
Published in David E. Wesson, Bindi Naik-Mathuria, Pediatric Trauma, 2017
The third area in the acute care setting that rehabilitation professionals may assist in is the identification and treatment of paroxysmal sympathetic hyperactivity (PSH). While the pathophysiology of TBI is beyond the scope of this chapter, the metabolic cascade of events after TBI has been documented to the extent of our current understanding by Giza and Hovda and Maxwell [31, 32]. It is likely that this metabolic cascade is closely associated with the poorly understood consequence of TBI most recently known as PSH. In 2014, Baguley et al., using the Delphi method, published a consensus statement on defining the PSH syndrome, diagnostic criteria, and a proposed tool for future research (Figure 22.1) [33].
Clinical management of the minimally conscious state
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Yelena G. Bodien, Sabrina R. Taylor, Joseph T. Giacino
During inpatient rehabilitation, more than 80% of DOC patients experience at least one medical complication.70 Consequently, it is essential that rehabilitation efforts focus on the identification and management of complications associated either directly with the brain injury (i.e., paroxysmal sympathetic hyperactivity, tone, and contractures) or with prolonged immobility and hospitalization (i.e., infection). Paroxysmal sympathetic hyperactivity (or dysautonomia), infection, and hypertonus are among the most common complications. Dysautonomia is a disturbance of the sympathetic nervous system that includes markedly increased heart rate, respiratory rate, blood pressure, and diaphoresis. Pharmaceutical agents such as morphine and beta-blockers may prevent these symptoms; however, these medications may also have sedative properties that decrease behavioral output and can mask level of conscious awareness. Nonpharmaceutical treatment may include environmental management and avoidance of triggers that lead to episodes of storming. Aspiration pneumonia, which is associated with tracheostomy, swallowing disorders, and diminished cough reflex, requires readmission to an acute care setting and may be life threatening. Elevating the head of the bed, modifying feeding schedules, and frequent oral care can help prevent episodes of aspiration pneumonia71 (see also http://www.aacn.org/wd/practice/docs/practicealerts/prevention-aspiration-practice-alert.pdf?menu=aboutus). Spasticity and contractures, apart from being painful, may limit the capacity to respond to motor commands, leaving a false impression of failure to comprehend language or inability to initiate behavioral activity. There is some evidence that these symptoms may be managed with passive range-of-motion and serial casting, pharmacological agents (i.e., botulin toxin, baclofen), and other medical interventions, such as tendon lengthening.72
Continuum of care and longitudinal recovery in a 17-year-old athlete with second impact syndrome
Published in Brain Injury, 2023
Nabela Enam, Hansen Deng, Nicholas S. Race, Dewan S. Majid, David O. Okonkwo, Kevin M. Franzese
The patient was extubated on post-trauma day #7. On post-trauma day #11, the physiatry team evaluated the patient. He was alert but non-verbal and not following commands, with occasional left-sided purposeful movements and right hemiparesis. The exam was consistent with a minimally conscious state minus the ability to communicate (MCS-). He had intermittent tachycardia, hypertension, and fevers concerning for paroxysmal sympathetic hyperactivity (PSH). The patient was placed on a cooling blanket and started on propranolol, clonidine, and gabapentin after infection was ruled out. Low dose bromocriptine was recommended for dual benefit of neurostimulation and concern for overlapping PSH. Trazodone was initiated for sleep-wake cycle regulation. Within a week, the patient showed improved arousal and participation.
Evaluation of rest-activity cycles in patients with severe acquired brain injury: an observational study
Published in Brain Injury, 2021
Simon Kjeldsen, Jørgen Feldbæk Nielsen, Ole Kæseler Andersen, Iris Brunner
All patients admitted to the ward were screened for eligibility. To be eligible, patients were required to have a diagnosis consistent with an sABI. Eligible patients had to be classified as being >II and ≤ VII on the Rancho Los Amigos Score (RLAS) (25,26) and ≥18 years old. Furthermore, relatives/surrogates able to give informed consent had to be available. Patients were excluded if they had an expected stay shorter than 3 weeks, or if they presented with spinal lesions, terminal illness, or polyneuropathies (e.g., Guillain-Barrés) as their primary diagnosis. An additional exclusion criterion was the presence of paroxysmal sympathetic hyperactivity based on physician and team evaluation. Furthermore, patients with no or very little motor activity due to either locked-in syndrome or severe tetraparesis were excluded as their ACC data would not reflect rest and activity. The threshold for exclusion due to a lack of motor activity was set at two times the standard deviation of the average vector magnitude pr. Twenty-four hour of subjects with locked-in syndrome or RLAS ≤ II.
Clinical characteristics and prognosis of paroxysmal sympathetic hyperactivity in patients with severe nontraumatic brain injury
Published in Brain Injury, 2023
He Miao, Huijin Huang, Weibi Chen, Ying-Ying Su, Yan Zhang
Paroxysmal sympathetic hyperactivity (PSH) is a syndrome recognized in a subgroup of survivors of severe acquired brain injury who exhibit simultaneous paroxysmal transient increases in sympathetic (increased heart rate, blood pressure, respiratory rate, temperature, and sweating) and motor (posturing) activity (1). Penfield was the first reported on this syndrome in 1929 (2), the phenomenon has since become widely recognized, and Rabinstein named the syndrome ‘PSH’ in 2007 (3). Since PSH can lead to unstable vital signs and even life-threatening symptoms, an increasing number of doctors in neurology and critical care are paying attention to it. Most studies of PSH investigate severe traumatic brain injury (TBI), although some studies have explored other causes, such as hypoxia or stroke, and rare causes, including hydrocephalus, tumor, hypoglycemia, anti-N-methyl-D-aspartate (NMDA) receptor encephalitis, cryptococcal meningitis, tuberculous meningitis, and acute disseminated encephalomyelitis (ADEM) (4–11). However, our clinical understanding of PSH in patients with severe nontraumatic brain injury is clearly insufficient. Moreover, because of the nonspecific clinical characteristics of PSH, the symptoms of which are often confused with those of fever and epilepsy in severe patients, there is a risk of misdiagnosis and delayed treatment in clinical practice. Moreover, there is some controversy about whether PSH is related to the prognosis in patients with severe disease. Therefore, our study was performed to actively explore the clinical and prognostic characteristics of PSH in patients with severe nontraumatic brain injury to improve the ability to identify and correctly treat PSH as soon as possible.